Genetic interactions of pokkuri with seven in absentia, tramtrack and downstream components of the sevenless pathway in R7 photoreceptor induction in Drosophila melanogaster.

Abstract

The sevenless (sev) cascade plays an inductive role in formation of the R7 photoreceptor, whilst the pokkuri (pok) and tramtrack (ttk) gene products are known to repress R7 induction in developing ommatidia of Drosophila melanogaster. To elucidate how these positive and negative signalling mechanisms co-operate in the normal fate determination of R7, genetic interactions of mutations in the pok locus with ttk and downstream elements of sev including Gap1, raf1, rolled (r1) and seven in absentia (sina) were examined. The eye phenotype of a weak hypomorph, pok ¹⁵, was enhanced dominantly by Gap1-^mip, a recessive mutation in a gene encoding a down-regulator of Ras1, producing multiple R7 in ommatidia. Ras1 has been reported to activate r1-encoded mitrogen-activated protein (MAP) kinase via Raf1 that is associated physically with Rasl. Ommatidia of raf1 ^c110 and rl ²/rl^EMS64 typically lacked R7 and a few outer photoreceptors. The pok ¹ mutation suppressed dominantly the rafl ^c110 rl²/rl^EMS64 eye phenotypes, allowing single R7 cells to develop in ommatidia. The rafl ^c110 mutation improved adult viability of pok ¹ homozygotes. An in vitro experiment demonstrated that MAP kinase phosphorylates Pok protein. Ttk is a transcriptional repressor which binds to the regulatory sequence upstream of the fushi-tarazu (ftz), even skipped (eve) and engrailed (en) coding region. A reduced activity in ttk resulted in enhancement of the pok phenotype. ttk mutations produced extra R7 cells even in sina homozygotes whilst the pok mutation did not. This result indicates that Ttk represses R7 induction downstream of the sites where Pok and Sina function.